VCAM1 and ICAM1 expression in oral lichen planus.

Oral lichen planus is a chronic inflammatory immune-mediated disease. ICAM-1 and VCAM-1 are vascular adhesion molecules that their receptors are located on endothelial cells and leukocytes. The aim of this study is the immunohistochemical evaluation of VCAM1 and ICAM1 in oral lichen planus and to compare these two markers with normal mucosa for evaluation of angiogenesis. This descriptive-analytical study was performed on 70 paraffined blocks of oral lichen planus and 30 normal mucosa samples taken from around the lesions. Samples were stained with H & E and then with Immunohistochemistry using monoclonal mouse anti human VCAM1 (CD106), & monoclonal mouse anti human ICAM1(CD54) for confirmation of diagnosis. Slides were evaluated under light microscope and VCAM1 and ICAM1 positive cells (endothelial cells and leukocytes) were counted. Data were analyzed with Mann-Whitney test, Wilcoxon and Chi-Square and p<0.001 was declared significant. VCAM1 and ICAM1 expression significantly increased compared to normal mucosa in oral lichen planus according to the percentage of stained cells (p=0.000& p=0.000, Mann-Whitney test). Thirty cases of oral normal mucosa associated with lichen planus showed that the VCAM1 has increased significantly in comparison to normal mucosa (p<0.001). Also, ICAM1 expression between lichen planus and normal mucosa, showed a significantly difference (p<0.001). A significant difference between VCAM1 and ICAM1 expression and type of lichen planus was not observed (p>0.05). Regarding the results, it seems that high expression of VCAM1 and ICAM1 is related to oral lichen planus.

ichen planus is a relatively common chronic inflammatory disease of the skin that mainly involves the oral mucosa. The disorder was named by the English physician Erasmus Wilson (1). With a prevalence of 1 to 2 percent, it has been indicated to be more frequent among females (2). Recent evidence suggests that the disease is an immune- considered as a consequence of immune response to antigenic variations (3)(4)(5)(6).
Lichen planus-triggering factor is unknown.
Although it has been established that the presence of lymphocytes is necessary and increase in vascular adhesion molecules and cytokines are required for lymphocyte accumulation at a certain site, there is a supporting hypothesis indicating that the main mechanism for lichen planus is lymphocyte activation by increasing vascular adhesion factors, such as ELAM1, VCAM1, ICAM1, and lymphocytic infiltration through increase in L-selectin, LFA-1 and VLA4 receptors (7). Vascular adhesion factors are the proteins that provide interaction between leukocytes and endothelium. Studies have shown that the expression of adhesion molecules has been changed in oral lichen planus. VCAM1 and ICAM1 are vascular adhesion molecules that allow leukocytes to adhere to the vessel wall (8,9).
Under normal conditions, small amount of ICAM1 is expressed by endothelial cells, monocytes and lymphocytes. Although ICAM1induced cytokines are increased in the sites of inflammation, VCAM1 also mediates primary adhesion of leukocytes and their migration from blood vessels and this action is reinforced by ICAM1 (8,9). VCAM1 (CD106) is one of the major vascular adhesion mediators directing the immune response (7,10); it is composed of immunoglobulin chains that express in cytokinestimulated large and small vessels (11). ICAM1 (CD54) is a single-chain glycoprotein on the surface of endothelial cells and immune system that stimulates immunological and inflammatory reactions (11,12).
There is an increase in ICAM1 expression in inflammatory conditions with specific inflammatory mediators. This human antigen is observed in endothelial and other epithelial cells.
ICAM1 binds to LFA1 and the latter, consisting of α and β subunits, is a member of the integrin family and a cell receptor; binding of ICAM1 and LFA1 can stimulate several reactions including T-cell specific responses to antigens as well as leukocytes binding to the endothelium and their migration (9,13). It is believed that some of cytokines such as lichen planus is stressed. Therefore, the present study was carried out to evaluate angiogenesis in lichen planus using immunohistochemical method.

Materials and Methods
This descriptive-analytical study was implemented on paraffined blocks of 70 samples expression in oral lichen planus and normal mucosa were examined and presented in Table 1 ( Fig. 1, 2 The highest VCAM1 and ICAM1 expression in lesions was observed for score 3; score 0 was found only in normal mucosa stained with VCAM1; however, for ICAM1, score 0 and 1 were observed. VCAM1 and ICAM1 expression was significantly more in lichen planus than normal mucosa. (p = 0.000, Mann-Whitney test)

Discussion
In the present study, VCAM1 and ICAM1 In conclusion, higher expression of VCAM1 and ICAM1 were seen in oral lichen planus compared to normal oral mucosa which appears to be involved in pathogenesis of oral lichen planus.
Moreover, evaluation of VCAM1 and ICAM1 in erosive and reticular lichen planus revealed no significant relationship between the type of lichen planus and the their expression.